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Background: The residual cardiovascular risk in subjects receiving guideline-recommended therapy is related to persistent vascular inflammation and IL-6 represents a target for its treatment. IL-6 binds to receptors on leukocytes and hepatocytes and/or by forming complexes with soluble IL-6 receptors (sIL-6R) binding to gp130 which is present on all cells. Here we aimed to estimate the associations of these two pathways with risk of cardiovascular disease (CVD)., Methods: IL-6 and sIL-6R were analyzed using the proximity extension assay. Baseline plasma samples were obtained from participants in the prospective Malmö Diet and Cancer (MDC) study (n = 4661), the SUMMIT VIP study (n = 1438) and the Carotid Plaque Imaging Project (CPIP, n = 285). Incident clinical events were obtained through national registers. Plaques removed at surgery were analyzed by immunohistochemistry and biochemical methods., Results: During 23.1 ± 7.0 years follow-up, 575 subjects in the MDC cohort suffered a first myocardial infarction. Subjects in the highest tertile of IL-6 had an increased risk compared to the lowest tertile (HR and 95% CI 2.60 [2.08-3.25]). High plasma IL-6 was also associated with more atherosclerosis, increased arterial stiffness, and impaired endothelial function in SUMMIT VIP, but IL-6 was only weakly associated with plaque inflammation in CPIP. sIL-6R showed no independent association with risk of myocardial infarction, atherosclerosis severity or vascular function, but was associated with plaque inflammation., Conclusions: Our findings show that sIL-6R is a poor marker of CVD risk and associated vascular changes. However, the observation that sIL-6R reflects plaque inflammation highlights the complexity of the role of IL-6 in CVD., Competing Interests: Declaration of Competing Interest The authors have no conflict of interest to disclose., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Purpose: We aimed to assess prevalence, distribution, and intensity of in-vivo arterial wall fibroblast activation protein (FAP) uptake, and its association with calcified plaque burden, cardiovascular risk factors (CVRFs), and FAP-avid tumor burden., Methods: We analyzed 69 oncologic patients who underwent [ 68  Ga]Ga-FAPI-04 PET/CT. Arterial wall FAP inhibitor (FAPI) uptake in major vessel segments was evaluated. We then investigated the associations of arterial wall uptake with calcified plaque burden (including number of plaques, plaque thickness, and calcification circumference), CVRFs, FAP-positive total tumor burden, and image noise (coefficient of variation, from normal liver parenchyma)., Results: High focal arterial FAPI uptake (FAPI +) was recorded in 64/69 (92.8%) scans in 800 sites, of which 377 (47.1%) exhibited concordant vessel wall calcification. The number of FAPI + sites per patient and (FAPI +)-derived target-to-background ratio (TBR) correlated significantly with the number of calcified plaques (FAPI + number: r = 0.45, P < 0.01; TBR: r =  - 0.26, P = 0.04), calcified plaque thickness (FAPI + number: r = 0.33, P < 0.01; TBR: r =  - 0.29, P = 0.02), and calcification circumference (FAPI + number: r = 0.34, P < 0.01; TBR: r =  - 0.26, P = 0.04). In univariate analysis, only body mass index was significantly associated with the number of FAPI + sites (OR 1.06; 95% CI, 1.02 - 1.12, P < 0.01). The numbers of FAPI + sites and FAPI + TBR, however, were not associated with other investigated CVRFs in univariate and multivariate regression analyses. Image noise, however, showed significant correlations with FAPI + TBR (r = 0.30) and the number of FAPI + sites (r = 0.28; P = 0.02, respectively). In addition, there was no significant interaction between FAP-positive tumor burden and arterial wall FAPI uptake (P ≥ 0.13)., Conclusion: [ 68  Ga]Ga-FAPI-04 PET identifies arterial wall lesions and is linked to marked calcification and overall calcified plaque burden, but is not consistently associated with cardiovascular risk. Apparent wall uptake may be partially explained by image noise., (© 2023. The Author(s).)

We report that people with human immunodeficiency virus (HIV) diagnosed with coronary artery atherosclerotic plaques display higher levels of HIV DNA compared with those without atherosclerotic plaques. In a multivariable prediction model that included 27 traditional and HIV-related risk factors, measures of HIV DNA were among the most important predictors of atherosclerotic plaque formation., Competing Interests: Potential conflicts of interest. J.-G. B. reports consulting fees paid to the author not related to this work from Gilead Sciences, Merck, and ViiV healthcare; payment for lectures not related to this work from Gilead Science and Merck. C. C.-L. reports grants or contracts unrelated to this work from Fonds de recherche santé Québec and Réseau SIDA-MI. M. D. is a member of the steering committee of the Canadian HIV Clinical Trial Network. M. E.-F. reports funding through NIH #R01AG054324. M.-A. J. reports funds from the Canadian Institutes of Health Research (CIHR), Team Grant #HAL-157985, as part of the Canadian HIV and aging study. C. L. T. reports grants or contracts from Merck, Gilead, CIHR, and NIH; consulting fees from Merck, GSK, Medicago, Gilead, AstraZeneca, and Moderna; payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events from Merck, GSK, AstraZeneca, Gilead, Pfizer, Sanofi; support for attending meetings and/or travel from Moderna; participation on a Data Safety Monitoring Board or Advisory Board for Colcorona, Dalcor, and Hesperidin. All other authors report no potential conflicts. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed., (© The Author(s) 2022. Published by Oxford University Press on behalf of Infectious Diseases Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: Rates of cardiovascular disease are higher in people living with HIV. Early detection of high-risk subjects (applying cardiovascular risk equations) would allow preventive actions. D:A:D, ASCVD, and FRS:CVD equations are the most recommended. However, controversies surround these equations and cut-points, which have the greatest capacity to discriminate high-risk subjects., Objectives: The study aims (i) to assess the association/agreement between cardiovascular risk levels obtained with D:A:D and fifteen other cardiovascular risk equations, (ii) to detect cardiovascular risk equation's capability to detect high-risk subjects, and (iii) to specify the optimal cardiovascular risk equation´s cut points for the prediction of carotid plaque presence, as a surrogate of high cardiovascular risk., Methods: 86 adults with HIV were submitted to the clinical, laboratory, and cardiovascular risk evaluation (including carotid ultrasound measurements). Cardiovascular risk was evaluated through multiple risk equations (e.g., D.A.D, ASCVD, and FRS equations). Association and agreement between equations (Correlation, Bland-Altman, Williams´test) and equation's capacity to detect plaque presence (ROC curves, sensitivity, specificity) were evaluated., Results: Cardiovascular risk equations showed a significant and positive correlation with plaque presence. Higher high-cardiovascular risk detection capability was obtained for ASCVD and D:A:D. Full D:A:D5y>0.88 %, ASCVD>2.80 %, and FRS:CVD>2.77 % correspond to 80 % sensitivity., Conclusion: All cardiovascular risk equations underestimate the true risk in HIV subjects. The cut-- points for high cardiovascular risk were found to vary greatly from recommended in clinical guidelines., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Objectives: This study aimed to determine the correlation of [ 68 Ga]Ga-NODAGA ZOL uptake in atherosclerotic plaques and the cardiovascular risk profile of patients imaged with positron emission tomography (PET), wherein quantification of uptake was determined by atherosclerotic plaque maximum target-to-background ratio (TBRmax). We also correlated uptake with a history of cardiovascular events., Methods: We included patients who underwent PET/CT imaging post-injection of [ 68 Ga] Ga-NODAGA ZOL . We documented the number of atherosclerotic plaques found in the major arteries on CT and the cardiovascular risks in each patient. We quantified the intensity of tracer uptake in atherosclerotic plaque in the major arteries using the maximum standardized uptake value (SUVmax). The SUVmax of the most tracer-avid plaque was documented as representative of the individual arterial bed. We determined background vascular tracer activity using the mean standardized uptake value (SUVmean) obtained from the lumen of the superior vena cava. The maximum target-to-background ratio (TBRmax) was calculated as a ratio of the SUVmax to the SUVmean. The TBRmax was correlated to the number of atherogenic risk factors and history of cardiovascular events., Results: Thirty-four patients (M: F 31:3; mean age ± SD: 63 ± 10.01 years) with ≥ 2 cardiovascular risk factors were included. Statistically significant correlation between TBRmax and the number of cardiovascular risk factors was noted in the right carotid (r = 0.50; p < 0.05); left carotid (r = 0. 649; p < 0.05); ascending aorta (r = 0.375; p < 0.05); aortic arch (r = 0.483; p < 0.05); thoracic aorta (r = 0.644; p < 0.05); left femoral (r = 0.552; p < 0.05) and right femoral arteries (r = 0.533; p < 0.05). TBRmax also demonstrated a positive correlation to history of cardiovascular event in the right carotid (U = 26.00; p < 0.05); left carotid (U = 11.00; p < 0.05); ascending aorta (U = 49.00; p < 0.05); aortic arch (U = 37.00; p < 0.05); thoracic aorta (U = 16.00; p < 0.05); left common iliac (U = 49.500; p < 0.05), right common iliac (U = 43.00; p < 0.05), left femoral (U = 40.500; p < 0.05) and right femoral (U = 37.500; p < 0.05)., Conclusion: In this cohort of patients, a positive correlation was noted between atherosclerotic plaque uptake of [ 68 Ga]Ga-NODAGA ZOL and the number of atherogenic risk factors which translates to the risk of atherosclerosis and cardiovascular risk factors., (© 2022. The Author(s) under exclusive licence to The Japanese Society of Nuclear Medicine.)

Introduction: Classic cardiovascular risk factors do not explain all the cardiovascular events. Obstructive sleep apnoea (OSA) has been proposed as a potential and prevalent cardiovascular risk factor. Our study aimed to describe the prevalence of OSA in a middle-aged cohort with mild-moderate cardiovascular risk and evaluate its association with atherosclerotic disease., Methods: This is an observational cross-sectional ancillary study of the ILERVAS project which was aimed to study subclinical arterial disease in a cohort with mild-moderate cardiovascular risk. In a sample of consecutive subjects, we performed a sleep study and evaluate OSA prevalence and its association with carotid and femoral atheroma plaques and atherosclerotic burden., Results: Overall, 966 subjects with a median age of 57 years (25-75th percentile; 52-62) and a body mass index (BMI) of 28.5kg/m 2 (25.6-31.6) were included. Of these, 72.6% (69.7%-75.3%) had OSA (apnoea-hypopnoea index (AHI)≥5/h); 35.7% (32.8%-38.8%) had mild OSA (AHI 5-14.9/h) and 36.9% (33.9%-39.9%) had moderate/severe OSA (AHI≥15/h). Mean oxygen saturation and the percentage of time with oxygen saturation<90% (CT90) were associated with atherosclerotic burden (e β (95%CI) 0.932 (0.892, 0.974); 1.005 (1.002, 1.009), respectively) and total plaque (OR (95%CI) 0.88 (0.797,0.971); 1.013 (1.004,1.021), respectively). No association with the AHI or oxygen desaturation index was found., Conclusions: This study confirms a high prevalence of OSA in patients with mild-moderate cardiovascular risk and shows an association between atherosclerotic burden, total and femoral plaque with CT90 and mean oxygen saturation, suggesting the importance of OSA-related hypoxaemia in the induction of atherosclerotic disease., (Copyright © 2021 SEPAR. Published by Elsevier España, S.L.U. All rights reserved.)

Article Title and Bibliographic Information: Joshi, Chaitanya; Bapat, Ranjeet; Anderson, William; Joshi, Chaitanya; Bapat, Ranjeet; Anderson, William; Dawson, Dana; Hijazi, Karolin; Cherukara, George (2021). "Detection of periodontal microorganisms in coronary atheromatous plaque specimens of myocardial infarction patients: A systematic review and meta-analysis." Trends in Cardiovascular Medicine 31(1): 69-82., Source of Funding: None., Type of Study/design: Systematic review with meta-analysis of data., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Aims: We aimed to evaluate whether traditional risk scores [short-term, 'psoriasis-modified' (multiplied by 1.5) and lifetime] were able to capture high cardiovascular disease (CVD) risk as defined by the presence of atherosclerotic plaques in coronary, femoral, or carotid arteries in psoriasis., Methods and Results: We used two prospectives obseravational cohorts. European cohort: femoral and carotid atherosclerotic plaques were evaluated by ultrasound in 73 psoriasis patients. Lifetime CVD risk (LTCVR) was evaluated with QRISK-LT; short-term CVD risk was evaluated with SCORE and psoriasis-modified SCORE. American cohort: 165 patients underwent coronary computed tomography angiography to assess presence of coronary plaques. LTCVR was evaluated with atherosclerotic cardiovascular disease (ASCVD-LT) lifetime; short-term CVD risk was evaluated with ASCVD and psoriasis-modified ASCVD. European cohort: subclinical atherosclerosis was present in 51% of patients. QRISK-LT identified 64% of patients with atherosclerosis missing a high proportion (35%) with atheroma plaque (P < 0.05). The percentage of patients with atherosclerosis identified by QRISK-LT was significantly higher than those detected by SCORE (0%) and modified SCORE (10%). American cohort: subclinical atherosclerosis was present in 54% of patients. ASCVD-LT captured 54% of patients with coronary plaques missing a high proportion (46%) with coronary plaque (P < 0.05). The percentage of patients with atheroma plaques detected with ASCVD and modified ASCVD were only 20% and 45%, respectively., Conclusions: Application of lifetime, short-term and 'psoriasis-modified' risk scores did not accurately capture psoriasis patients at high CVD risk., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions, please email: journals.permissions@oup.com.)

Purpose: Cardiovascular disease (CVD) is the leading cause of death, globally, and its prevalence is only expected to rise due to the increasing incidence of co-morbidities such as obesity and diabetes. Medical treatment of CVD is directed primarily at slowing or reversing the underlying atherosclerotic process by managing circulating lipids with an emphasis on control of low-density lipoprotein (LDL) cholesterol. However, over the past several decades, there has been increasing recognition that chronic inflammation and immune system activation are important contributors to atherosclerosis. This shift in focus has led to the elucidation of the complex interplay between cholesterol and cellular secretion of cytokines involved in CVD pathogenesis. Of the vast array of cytokine promoting atherosclerosis, interferon (IFN)-γ is highly implicated and, therefore, of great interest., Methods: Literature review was performed to further understand the effect of IFN-γ on the development of atherosclerotic CVD., Results: IFN-γ, the sole member of the type II IFN family, is produced by T cells and macrophages, and has been found to induce production of other cytokines and to have multiple effects on all stages of atherogenesis. IFN-γ activates a variety of signaling pathways, most commonly the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway, to induce oxidative stress, promote foam cell accumulation, stimulate smooth muscle cell proliferation and migration into the arterial intima, enhance platelet-derived growth factor expression, and destabilize plaque. These are just a few of the contributions of IFN-γ to the initiation and progression of atherosclerotic CVD., Conclusion: Given the pivotal role of IFN-γ in the advancement of CVD, activation of its signaling pathways is being explored as a driver of atherosclerosis. Manipulation of this key cytokine may lead to novel therapeutic avenues for CVD prevention and treatment. A number of therapies are being explored with IFN-γ as the potential target.

Background: Cardiovascular disease is a major cause of death in post-liver transplantation (LT). The aim of this study was to evaluate LT patients as to the carotid intima-media thickness (CIMT) and its association with nutritional status, dietary intake, metabolic profile and cardiovascular risk factors., Methods: In this cross-sectional study, adult patients with more than 12 months of post-transplant follow-up underwent clinical, laboratory, functional and nutritional evaluation by 3-day-diet-record, anthropometry and dynamometry. CIMT was evaluated by Doppler ultrasonography., Results: Sixty-nine post-LT patients [males 61%, median of age 59 (51-64) years were included; median time post-liver transplantation 2.8 (1.4-6.3) years]. High prevalence of malnutrition was found (45% of arm muscle area < p15 and 71% of handgrip strength < p30). Excess weight was present in 72% of patients, body mass index ≥ 30 kg/m 2 in 35% and metabolic syndrome in 51%. Abnormal CIMT was found in 54% of the sample. Patients with abnormal CIMT presented higher cardiovascular risk Score, LDL cholesterol, higher prevalence of high-sensitive C-reactive protein ≥ 1 mg/L and higher intake of saturated and trans fatty acids (P < 0.05 for all)., Conclusions: Abnormal IMT was commonly found in LT patients presenting at the same time with overweight and dynapemia. These results were associated with higher LDL-cholesterol levels, high-sensitive C-reactive protein ≥ 1 mg/L and higher intake of saturated and trans fatty acids. Preventive measures, including dietary advice, are required for all post-liver transplantation patients to minimize cardiovascular risk., (Copyright © 2018 Elsevier Masson SAS. All rights reserved.)

Purpose of Review: This short review is intended primarily to summarize the understanding of the interrelated roles of endoplasmic reticulum (ER) stress, oxidative stress and inflammation in cardiovascular diseases., Recent Findings: Insults interfering with ER function lead to the accumulation of unfolded and misfolded proteins in the ER. An excess of proteins folding in the ER is known as ER stress. This condition initiates the unfolded protein response (UPR). When the UPR fails to control the level of unfolded and misfolded proteins, ER-initiated apoptotic signalling is induced. Moreover, the role of the protective nuclear erythroid-related factor 2 (Nrf2)/antioxidant-related element (ARE) and the activation of the pro-inflammatory nuclear factor-kappa B (NF-kB) are analysed. Authors summarize evidence that oxidative stress, inflammation and ER stress are closely entwined phenomena. They are involved in the pathogenesis of different cardiovascular diseases. Current literature data are presented, focusing on three topics of related pathologies: atherosclerotic plaque, coronary artery disease and diabetes. This review will provide a basic platform for study and application to several other conditions in which oxidative stress, ER stress and inflammation are key features. Future studies in this area may identify the most promising molecules to be investigated as common targets for cardiovascular diseases.

Background and Objectives: Chronic kidney disease (CKD) and atherosclerosis are 2 interrelated diseases that increase the risk of cardiovascular morbidity and mortality. The objectives of the ILERVAS project are: 1) to determine the prevalence of subclinical arterial disease and hidden kidney disease; 2) to assess the impact of early diagnosis of both diseases on cardiovascular morbidity and mortality and also on the progression of CKD; 3) to have a platform of data and biological samples., Methods: Randomized intervention study. From 2015 to 2017, 19,800 people (9,900 in the intervention group and 9,900 in the control group) aged between 45 and 70 years without previous history of cardiovascular disease and with at least one cardiovascular risk factor will be randomly selected from the primary health care centres across the province of Lérida. A team of experts will travel around in a mobile unit to carry out the following baseline tests on the intervention group: Artery ultrasound; (carotid, femoral, transcranial and abdominal aorta); ankle-brachial index; spirometry; determination of advanced glycation end products; dried blood spot and urine spot tests. Additionally, blood and urine samples will be collected and stored in the biobank to identify new biomarkers using omics studies. Participants will be followed up until 2025 for identification of cardiovascular events, treatment changes and changes in lifestyle., Conclusions: The ILERVAS project will reveal the prevalence of subclinical vascular disease and hidden kidney disease, determine whether or not their early diagnosis brings health benefits and will also allow investigation of new risk factors., (Copyright © 2016 Sociedad Española de Nefrología. Published by Elsevier España, S.L.U. All rights reserved.)

Objective Evidence from coronary imaging studies suggests an association between increased atherosclerotic plaque burden and cardiovascular disease (CVD) outcomes. A systematic review was performed to evaluate the relationship between coronary atherosclerotic plaque burden changes measured by intravascular ultrasound (IVUS) and CVD outcomes. Research design and methods Rigorous systematic review methodology was used to identify prospective studies of any design assessing the relationship between atherosclerotic plaque volume (percentage or total atheroma volume [PAV or TAV]) changes and CVD outcomes, using multivariable analyses. Main outcome measures CVD outcomes including major adverse cardiac events (MACEs) and major adverse cardiac and cerebrovascular events (MACCEs). Results Literature searches from inception to February 2015 retrieved 6958 records after de-duplication. From these four studies (14 papers) were included. One study reported a significantly lower rate of CVD outcomes associated with a greater reduction in PAV (hazard ratio [HR] 0.26, 95% confidence interval [CI] 0.07-0.83). One study reported that large plaque volume was significantly associated with a greater risk of major adverse cardiac events (MACEs) (HR 1.73, 95% CI: 1.02-2.96). Similarly, a third study reported a significant increase in MACE with an increase in baseline PAV (HR 1.51, 95% CI: 1.06-2.51). Only one potentially inadequately powered Japanese study did not find a statistically significant relationship between PAV changes and MACE. Conclusions The current evidence suggests an independent and statistically significant association between increases in coronary atherosclerotic plaque burden measured by IVUS and greater long-term risk of future CVD outcomes. However, this evidence comes from a limited number of studies which mainly focus on Japanese populations and populations after PCI. Further large prospective studies are required to confirm these findings.

Current diagnostic technique in direct identification of multi‐site plaques and simultaneous assessment of plaque vulnerability remains a challenge, which is crucial for indicating the risk of atherosclerotic cardiovascular diseases (ASCVD). Herein, an osteopontin (OPN)‐specific nanoprobe (OPN Ab‐Au/FeNiPO4@ICG) with both multiple spectra optoacoustic tomography (MSOT) and computed tomography (CT) imaging, is constructed successfully realizing systemic screening of vulnerable plaque. OPN Ab‐Au/FeNiPO4@ICG nanoprobe specifically targeted OPN‐overexpressed foam cells and recognized the vulnerable plaque at the molecular level. In AS mice, CT imaging exhibits that OPN Ab‐Au/FeNiPO4@ICG nanoprobe effectively avoid interference from calcification and accurately visualized AS plaque. MSOT functional imaging results reveals that after the injection of OPN Ab‐Au/FeNiPO4@ICG nanoprobe, the carotid plaque exhibited a much higher MSOT signal than the aortic arch plaque (P = 0.0291). Further pathological analysis displays that the carotid plaque possessed a much higher vulnerability score (P = 0.0247), in agreement with the MSOT signals. More importantly, the linear regression analysis confirms the high correlation between the MSOT signals and plaque vulnerability with R = 0.7095 (P = 0.0216), demonstrating the potential of the proposed nanoprobe in systematic evaluation of plaque vulnerability. This work employs the dual‐model nanoprobe strategy for both plaque localization and vulnerability assessment, greatly advancing the accurate diagnosis of ASCVD. [ABSTRACT FROM AUTHOR]

Background: Chronic kidney disease (CKD) is a significant public health concern associated with a high prevalence of carotid plaques, which are indicators of atherosclerosis and predictors of adverse cardiovascular outcomes. Inflammation is a hallmark of CKD, contributing to both renal dysfunction and cardiovascular complications. This study aims to investigate the association between inflammatory markers—systemic inflammatory response index (SIRI), systemic immune-inflammation index (SII), aggregate inflammatory status index (AISI), monocyte to high-density lipoprotein cholesterol ratio (MHR), neutrophil to high-density lipoprotein cholesterol ratio (NHR), neutrophil to lymphocyte ratio (NLR), and monocyte to lymphocyte ratio (MLR)—and carotid plaques in CKD patients, and to explore the potential mediating role of estimated glomerular filtration rate (eGFR) in this relationship. Methods: A cross-sectional analysis was conducted on patients admitted to the Division of Nephrology between January 2023 and June 2023. The primary endpoint was the presence of carotid plaques assessed using ultrasound imaging. Multivariable logistic regression models were used to examine the associations between inflammatory markers and carotid plaques, and trend tests were performed to evaluate the trending association of carotid plaques risk and inflammatory markers in tertiles. Restricted cubic spline (RCS) analysis was used to assess potential non-linear relationships, and subgroup analyses were conducted to examine consistency across different strata. Mediation analysis was performed to explore the role of eGFR. Results: Of the 609 participants, 387 were included in the final analysis after applying exclusion criteria. Elevated levels of LnSIRI (OR = 1.87, 95% CI = 1.25–2.80), LnSII (OR = 1.67, 95% CI = 1.09–2.56), LnAISI (OR = 1.70, 95% CI = 1.22–2.37), LnMHR (OR = 1.94, 95% CI = 1.15–3.26), LnNHR (OR = 1.82, 95% CI = 1.10–3.02), and LnMLR (OR = 2.26, 95% CI = 1.18–4.34) were significantly associated with the presence of carotid plaques. There were significant trends for increasing tertiles of SIRI, AISI, MHR and NHR. RCS analysis showed no significant non-linear associations. Subgroup analyses indicated similar associations across most strata. eGFR partially mediated these relationships, with proportions mediated ranging from 14.7 to 17.5%. Conclusions: Inflammatory markers are significantly associated with carotid plaques in CKD patients, with eGFR playing a partial mediating role. These findings highlighted the importance of managing inflammation and maintaining renal function to mitigate the risk of atherosclerosis in CKD patients. Trial registration: Not applicable. [ABSTRACT FROM AUTHOR]

Atherosclerosis, a term derived from the Greek "athero" (atheroma) and "sclerosis" (hardening), is a long-standing process that leads to the formation of atheromatous plaques in the arterial wall, contributing to the development of atherosclerotic cardiovascular disease. The proliferation and migration of vascular smooth muscle cells (VSMCs) and the switching of their phenotype play a crucial role in the whole process. Retinoic acid (RA), a natural derivative of vitamin A, has been used in the treatment of various inflammatory diseases and cell proliferation disorders. Numerous studies have demonstrated that RA has an important inhibitory effect on the proliferation, migration, and dedifferentiation of vascular smooth muscle cells, leading to a significant reduction in atherosclerotic lesions. In this review article, we explore the effects of RA on the pathogenesis of atherosclerosis, focusing on its regulatory action in VSMCs and its role in the phenotypic switching, proliferation, and migration of VSMCs. Despite the potential impact that RA may have on the process of atherosclerosis, further studies are required to examine its safety and efficacy in clinical practice. [ABSTRACT FROM AUTHOR]

Background: Cardiovascular diseases, particularly myocardial infarction (MI), are a major global health concern, with a rising incidence among younger populations. MI is a result of inadequate oxygen supply to the heart, often exacerbated by thrombus formation in coronary arteries due to atherosclerotic plaque deposition. Risk factors include obesity, hypertension, dyslipidaemia, diabetes mellitus, smoking, sedentary lifestyle, and familial predisposition. Early detection and intervention are crucial for improving prognosis and reducing mortality rates. Treatment strategies include pharmacotherapy and lifestyle modifications, with lifestyle interventions promoting physical activity and dietary changes. Aim: To determine the incidence and risk factors of Myocardial infarction among young adults. Methodology: This study investigated the prevalence and causes of myocardial infarction (MI) among patients admitted to the Department of Medicine at Adesh Hospital, Bathinda, Punjab. The sample size was 130, with participants being patients aged 18 and above, exhibiting cardiac manifestations, and providing consent for study participation. Data collection involved interactions with MI patients and their relatives, recording demographic information, smoking, and presenting symptoms. Data were analyzed using Microsoft Excel and SPSS version 28, with Chi square used for statistical significance. All data were collected after approval from the Institutional Ethics Committee. Result: The study involved 131 patients diagnosed with Myocardial Infarction (MI) at AIMSR, with 78.6% being males and a mean age of 56 ± 10.8 years. 15.2% of patients were young adults (<45 years). Risk factors included smoking, a positive family history of cardiovascular diseases, hypertension, and diabetes. Symptoms included chest pain, shortness of breath, and palpitations. Conclusion- study emphasizes the rising incidence of myocardial infarction (MI) among young adults, attributing it to factors such as smoking, socioeconomic status, rural residency, and comorbid conditions. It advocates for lifestyle changes, smoking cessation initiatives, and better healthcare access to mitigate this burden. Additionally, it calls for larger-scale studies to confirm these findings and develop tailored interventions for preventing and managing MI in young individuals. [ABSTRACT FROM AUTHOR]

Atherosclerosis is the foremost vascular disease, precipitating debilitating complications. Although therapeutic strategies have historically focused on reducing cholesterol deposition, recent insights emphasize the pivotal role of inflammation. Innate inflammation significantly contributes to plaque instability and rupture, underscoring the need for intervention across all disease stages. Numerous studies have highlighted the therapeutic potential of targeting innate immune pathways in atherosclerosis, revealing significant advancements in understanding the molecular mechanisms underlying inflammatory processes within arterial lesions. Notably, research has demonstrated that the modulation of microRNA‐146a (miR‐146a) expression impacts innate inflammation, effectively halts atherosclerosis progression, and enhances plaque stability by targeting interleukin‐1 receptor‐associated kinase (IRAK) and activating TNF receptor‐associated factor 6 (TRAF6), a signalling pathway involving toll‐like receptors (TLRs). Understanding the intricate mechanisms involved is crucial. This study provides a comprehensive analysis of the evidence and underlying mechanisms through which miR‐146a exerts its effects. Integrating these findings into clinical practice may herald a transformative era in managing atherosclerotic cardiovascular disease. [ABSTRACT FROM AUTHOR]

Dysbiosis within microbiomes has been increasingly implicated in many systemic illnesses, such as cardiovascular disease, metabolic syndrome, respiratory infections, and Alzheimer disease (Ad). The correlation between Ad and microbial dysbiosis has been repeatedly shown, yet the etiologic cause of microbial dysbiosis remains elusive. From a neuropathology perspective, abnormal (often age-related) changes in the brain, associated structures, and bodily lumens tend toward an accumulation of oxygen-depleted pathologic structures, which are anaerobically selective niches. These anaerobic environments may promote progressive change in the microbial community proximal to the brain and thus deserve further investigation. In this review, we identify and explore what is known about the anaerobic niche near or associated with the brain and the anaerobes that it is harbors. We identify the anaerobe stakeholders within microbiome communities and the impacts on the neurodegenerative processes associated with Ad. Chronic oral dysbiosis in anaerobic dental pockets and the composition of the gut microbiota from fecal stool are the 2 largest anaerobic niche sources of bacterial transference to the brain. At the blood-brain barrier, cerebral atherosclerotic plaques are predominated by anaerobic species intimately associated with the brain vasculature. Focal cerebritis/brain abscess and corpora amylacea may also establish chronic anaerobic niches in direct proximity to brain parenchyma. In exploring the anaerobic niche proximal to the brain, we identify research opportunities to explore potential sources of microbial dysbiosis associated with Ad. [ABSTRACT FROM AUTHOR]

Background: Cardiovascular disease is a major cause of morbidity in an aging HIV population. However, risk estimation with the most frequent equations usually classifies HIV patients as having a low or moderate risk. Several studies have described a very high prevalence of subclinical atherosclerosis in a middle-aged, non-HIV population. There is insufficient body of knowledge to understand if this is the case in people living with HIV (PLWH). We aim to calculate the proportion of patients with subclinical atherosclerosis in a single site cohort of HIV-infected subjects. Methods: We have analyzed chronically HIV infected adults (≥ 18 years) who were on active follow-up in an HIV unit specialized in the care of cardiovascular health. The most recent clinical visit and vascular ultrasonography were used to assess the objectives of our research. Our primary objective was to describe the proportion of participants with subclinical atherosclerosis (focal protrusion into the lumen > 0.5 mm or > 50% of the surrounding IMT or a diffuse thickness > 1.5 mm) in a single site cohort of PLWH. Carotid and iliofemoral territories were evaluated. As a secondary objective we have run a multivariate analysis to determine which HIV and non-HIV factors might be related with the presence of atherosclerotic plaques. Findings We included a total of 463 participants between November 2017 to October 2019. Subjects were predominantly male (84.2%) with a mean age of 48.8 years (SD 10.7). Hypercholesterolemia (36%) was the most prevalent comorbidity followed by Hypertension (18%) and Hypertriglyceridemia (16%). Mean duration of HIV infection is 12.3 years. Overall, participants had been receiving cART for a median of 9.5 years. Subclinical atherosclerosis was found in 197 subjects (42.5%; CI 95% [38.0–47.2]). The disease was found more frequently in the femoral arteries (37.8%) than in the carotid vascular bed (18.6%). Despite some HIV factors correlated with the presence of plaques in a univariate analysis (e.g., time with HIV-1 RNA > 50 copies/mL or time from HIV diagnosis), the only two explanatory factors that remained associated with the presence of atherosclerotic plaques in the multivariate analysis were smoking (OR 5.47, 95% CI 3.36 – 8.90) and age (OR 1.13, 95%CI 1.10 – 1.16). Interpretation We have found a very high prevalence of subclinical atherosclerosis among our cohort of PLWH. Despite having analyzed several HIV factors, age and smoking have been found to be the only factors associated with the development of atherosclerotic plaques. [ABSTRACT FROM AUTHOR]

Background and Purpose Experimental Approach Key Results Conclusion and Implications Elevated levels of 5‐HT have been correlated with coronary artery disease and cardiac events, suggesting 5‐HT is a potential novel factor in the development of atherosclerotic cardiovascular disease. However, the underlying pathological mechanisms of the 5‐HT system in atherosclerosis remain unclear. The 5‐HT2B receptor (5‐HT2BR), which establishes a positive feedback loop with 5‐HT, has been identified as a contributor to pathophysiological processes in various vascular disorders. In this study, we investigated the immunological impact of 5‐HT2BR in atherosclerosis‐prone apolipoprotein E‐deficient (ApoE−/−) mice.Plasma levels of 5‐HT were measured in mice using an ELISA kit. Atherosclerotic plaque formation, macrophage infiltration and inflammatory signalling were assessed in ApoE−/− mice by employing both pharmacological inhibition and genetic deficiency of 5‐HT2BR. Inflammasome activation was elucidated using peritoneal macrophages isolated from 5‐HT2BR‐deficient mice.An upregulation of 5‐HT2BR expression was observed in the aortas of ApoE−/− mice, exhibiting a strong correlation with the presence of macrophages in plaques. Atherosclerosis was attenuated in mice through pharmacological inhibition and genetic deficiency of 5‐HT2BR. Additionally, a significant reduction in atherosclerotic plaque size was achieved through bone marrow reconstitution with 5‐HT2BR‐deficient cells. 5‐HT2BR‐deficient macrophages showed attenuated interferon (IFN) signalling, NLRP3 inflammasome activation, and interleukin‐1β release. Moreover, macrophages primed with 5‐HT2BR deficiency displayed an anti‐inflammatory phenotype.These findings support the hypothesis that 5‐HT2BR in macrophages plays a causal role in the development of atherosclerosis, revealing a novel perspective for potential therapeutic strategies in atherosclerosis‐related diseases. [ABSTRACT FROM AUTHOR]

Objective • To explore the relationship between Serum amyloid protein A(SAA), lipoprotein-associated Phospholipase A2 (Lp-PLA2) and soluble CD40 ligand (sCD40L) in detecting the stability of carotid Atherosclerosis plaque. Methods • We examined 90 patients admitted to our hospital with acute cerebral infarction from July 2020 to December 2022. Carotid artery ultrasounds were performed for all of them. These patients were then divided into two groups: the stable plaque group (45 cases) and the unstable plaque group (45 cases), based on the ultrasound results. Additionally, we included a control group of 30 healthy individuals from our hospital. We collected fasting blood samples from the patients upon admission and used enzyme-linked immunosorbent assays to measure the mass concentrations of sCD40L, Lp-PLA2, and SAA in their serum. The results of these biomarkers were compared and analyzed to assess potential associations with plaque stability in patients with cerebral infarction. Results • Comparison of general clinical data and laboratory data: except for High-density lipoprotein, there was a statistical difference between the control group and the cerebral infarction group (P < .05), there was no statistical difference in gender, smoking history, drinking history and age (P > .05). Compared with the control group, the mass concentrations of sCD40L, Lp-PLA2, and SAA in patients with stable and unstable plaques increased significantly (P < .05); Compared with the stable plaque group, the mass concentrations of sCD40L, Lp-PLA2, and SAA in unstable plaque patients increased with statistical significance (P < .05). Correlation analysis shows that the mass concentrations of sCD40L, Lp-PLA2, and SAA are positively correlated with the stability of carotid artery plaques. SCD40L, Lp-PLA2 and SAA have certain diagnostic significance in the subject’s working characteristic curve (Receiver operating characteristic) as a marker molecule for the diagnosis of unstable plaque. sCD40L (AUC=0.883) has more diagnostic value than SAA (AUC=0.756) and Lp-PLA2 (AUC=0.826). A binary logistic regression analysis was conducted using the stability of carotid artery plaques as the dependent variable and sCD40L, Lp-PLA2, and SAA as independent variables. The results showed that elevated serum sCD40L, Lp-PLA2, and SAA were independent risk factors for unstable carotid artery plaques (P < .05). Conclusion • The concentrations of sCD40L, Lp-PLA2 and SAA are closely related to the formation and type of carotid Atherosclerosis plaque in patients with acute cerebral infarction. This has potentially important clinical implications for the management and prevention of cardiovascular disease. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a highly prevalent condition associated with lipid accumulation in the intima layer of arterial blood vessels. The development of atherosclerotic plaques is associated with the incidence of major cardiovascular events, such as acute coronary syndrome or ischemic stroke. Due to the significant prevalence of atherosclerosis and its subclinical progression, it is associated with severe and potentially lethal complications. The pathogenesis of atherosclerosis is complex and not entirely known. The identification of novel non-invasive diagnostic markers and treatment methods that could suppress the progression of this condition is highly required. Non-coding RNA (ncRNA) involves several subclasses of RNA molecules. microRNA (miRNA), long non-coding RNA (lncRNA), and circular RNA (circRNA) differently regulate gene expression. Importantly, these molecules are frequently dysregulated under pathological conditions, which is associated with enhanced or suppressed expression of their target genes. In this review, we aim to discuss the involvement of ncRNA in crucial mechanisms implicated in the pathogenesis of atherosclerosis. We summarize current evidence on the potential use of these molecules as diagnostic and therapeutic targets. [ABSTRACT FROM AUTHOR]

Context The excess risk of fatal and nonfatal cardiovascular events is roughly twice as high in women than in men with type 1 diabetes. Objective To evaluate the impact of preeclampsia and parity on sex-based discrepancies in preclinical atherosclerosis and on the diagnostic performance of a cardiovascular risk scale. Design Cross-sectional study. Setting Single tertiary hospital. Patients A total of 728 people with type 1 diabetes (48.5% women) without cardiovascular disease and age ≥40 years, nephropathy, and/or ≥10 years of diabetes duration with another risk factor. Intervention Standardized carotid ultrasonography. Main Outcome Measures Carotid plaque determined by ultrasonography and cardiovascular risk estimated according to the Steno T1 Risk Engine (Steno-Risk). Results Nulliparous women and parous women without previous preeclampsia had a lower risk for carotid plaque than men (adjusted odds ratio:.48, 95% confidence interval [.28-.82]; adjusted odds ratio:.51 [.33-.79], respectively), without differences in the preeclampsia group. The prevalence of carotid plaque increased as the estimated cardiovascular risk increased in all subgroups except for preeclampsia group. The area under the curve of the Steno-Risk for identifying ≥2 carotid plaques was lower in the preeclampsia group (men:.7886; nulliparous women:.9026; women without preeclampsia:.8230; preeclampsia group:.7841; P between groups =.042). Neither the addition of parity nor preeclampsia in the Steno-Risk led to a statistically significant increase in the area under the curve. Conclusion The risk for carotid plaque in women compared with men decreased as exposure to obstetric factors diminished. However, the addition of these factors did not improve the prediction of the Steno-Risk. [ABSTRACT FROM AUTHOR]

Background. One of the most frequent causes of death is considered to be stroke on the back of atherosclerosis of the extracranial carotid arteries. Detection of atherosclerosis at an early stage facilitates timely prevention and reduces the risk of developing of an acute cardiovascular event in the future. Purpose. To evaluate the clinical significance of ultrasound in the diagnosis of atherosclerotic changes in the brachiocephalic arteries in people of different age groups. Materials and methods. Echography of brachiocephalic arteries was performed among 155 people aged 45 to 89 years, who were randomized into 3 age groups. The middle–aged group included 56 people; the elderly group – 54 people; the senile group - 45 people. The processing of the results of the study was carried out in the programs Statistica 10 (StatSoft, USA). Results. According to the data of sonography, atherosclerotic plaques were detected in 62.5% of the middle–aged group, 83.3% of the elderly group and 88.9% of senile age. Heterogeneous hypoechoic and calcified plaques are found only among people who are over 60 years old. Moderate stenosis was observed at the bifurcation of the common carotid artery in all age groups. Pronounced stenosis and critical vascular stenosis in the proximal part of the internal carotid artery are observed in senile age. The index of the maximum systolic velocity among people with atherosclerosis decreases with age. With increasing age, the level of vascular resistance increases. Conclusion. Considering significant changes in the indicators of atherosclerotic manifestations already in middle age, in order to reduce the increase in population mortality from cardiovascular diseases, the healthcare system should introduce early ultrasound screening of brachiocephalic arteries for patients from 18 years of age.

Background: Depression is the most common mental illness worldwide and generates an enormous health and economic burden. Furthermore, it is known to be associated with an elevated risk of arteriosclerotic cardiovascular diseases (ASCVD), particularly stroke. However, it is not a factor reflected in many ASCVD risk models, including SCORE2. Thus, we analysed the relationship between depression, ASCVD and SCORE2 in our cohort. Methods: We analysed 9350 subjects from the Paracelsus 10,000 cohort, who underwent both a carotid artery ultrasound and completed a Beck Depression Inventory (BDI) screening. Patients were categorised binomially based on the BDI score. Atherosclerotic carotid plaque or absence was dichotomised for logistic regression modelling. Odds ratios and adjusted relative risks were calculated using Stata. Results: Subjects with an elevated BDI (≥14) had higher odds for carotid plaques compared to subjects with normal BDI, especially after adjusting for classical risk factors included in SCORE2 (1.21; 95%CI 1.03–1.43, p = 0.023). The adjusted relative risk for plaques was also increased (1.09; 95%CI 1.01–1.18, p = 0.021). Subgroup analysis showed an increased odds of plaques with increases in depressive symptoms, particularly in women and patients ≤55 yrs. Conclusions: In our cohort, the BDI score is associated with subclinical atherosclerosis beyond classical risk factors. Thus, depression might be an independent risk factor which may improve risk stratification if considered in ASCVD risk prediction models, such as SCORE2. Furthermore, reminding clinicians to take mental health into consideration to identify individuals at increased atherosclerosis risk may provide added opportunities to address measures which can reduce the risk of ASCVD. [ABSTRACT FROM AUTHOR]

Background: Physical activity has been shown to have an effect on Carotid plaque (CP) which is a predictor of Cardiovascular disease (CVD). Studies have shown that physical activity can alter the composition of gut microbiota, whether its influence on CP was mediated by gut microbiota has yet to be proved. Methods: We conducted a case–control study involving 30 CP patients and 31 controls. Logistic regression was used to analyze the association between CP and physical activity. LefSe was used to explore the association between gut microbiota and physical activity as well as CP, and PhyloMed was used to examine the mediating effect of gut microbiota in the association between physical activity and CP. Results: After adjusting for potential confounders, adequate physical activity showed a significant association with a decreased risk of CP (ORadj: 0.25, 95%CI: 0.06, 0.97). CP was associated with enrichment in the order Bacteroidales within the phylum Bacteroidetes and the predominant microbiota in individuals without plaque was the order Clostridiales (LDA scores >3). Individuals with adequate physical activity had a higher abundance of the order Clostridiales, while the order Bacteroidetes was enriched in individuals with inadequate physical activity (LDA scores >3). The PhyloMed revealed a significant mediation effect of gut microbiota in the association between physical activity and CP (p  =  0.03). Conclusion: Adequate physical activity was significantly associated with a decreased risk of CP, and this association was mediated by an increase in the abundance of gut microbiota in the order Clostridiales. [ABSTRACT FROM AUTHOR]

Atherosclerosis (AS) is considered to be one of the major causes of cardiovascular disease. Its pathological microenvironment is characterised by increased production of reactive oxygen species, lipid oxides, and excessive inflammatory factors, which accumulate at the monolayer endothelial cells in the vascular wall to form AS plaques. Therefore, intervention in the pathological microenvironment would be beneficial in delaying AS. Researchers have designed biomimetic nanomedicines with excellent biocompatibility and the ability to avoid being cleared by the immune system through different therapeutic strategies to achieve better therapeutic effects for the characteristics of AS. Biomimetic nanomedicines can further enhance delivery efficiency and improve treatment efficacy due to their good biocompatibility and ability to evade clearance by the immune system. Biomimetic nanomedicines based on therapeutic strategies such as neutralising inflammatory factors, ROS scavengers, lipid clearance and integration of diagnosis and treatment are versatile approaches for effective treatment of AS. The review firstly summarises the targeting therapeutic strategy of biomimetic nanomedicine for AS in recent 5 years. Biomimetic nanomedicines using cell membranes, proteins, and extracellular vesicles as carriers have been developed for AS. [ABSTRACT FROM AUTHOR]

High-density lipoprotein (HDL) is a group of small, dense, and protein-rich lipoproteins that play a role in cholesterol metabolism and various cellular processes. Decreased levels of HDL and HDL dysfunction are commonly observed in individuals with type 2 diabetes mellitus (T2DM), which is also associated with an increased risk for cardiovascular disease (CVD). Due to hyperglycemia, oxidative stress, and inflammation that develop in T2DM, HDL undergoes several post-translational modifications such as glycation, oxidation, and carbamylation, as well as other alterations in its lipid and protein composition. It is increasingly recognized that the generation of HDL modifications in T2DM seems to be the main cause of HDL dysfunction and may in turn influence the development and progression of T2DM and its related cardiovascular complications. This review provides a general introduction to HDL structure and function and summarizes the main modifications of HDL that occur in T2DM. Furthermore, the potential impact of HDL modifications on the pathogenesis of T2DM and CVD, based on the altered interactions between modified HDL and various cell types that are involved in glucose homeostasis and atherosclerotic plaque generation, will be discussed. In addition, some perspectives for future research regarding the T2DM-related HDL modifications are addressed. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a common form of cardiovascular disease, which is one of the most prevalent causes of death worldwide, particularly among older individuals. Surgery is the mainstay of treatment for severe stenotic lesions, though the rate of restenosis remains relatively high. Current medication therapy for atherosclerosis has limited efficacy in reversing the formation of atherosclerotic plaques. The search for new drug treatment options is imminent. Some potent medications have shown surprising therapeutic benefits in inhibiting inflammation and endothelial proliferation in plaques. Unfortunately, their use is restricted due to notable dose-dependent systemic side effects or degradation. Nevertheless, with advances in nanotechnology, an increasing number of nano-related medical applications are emerging, such as nano-drug delivery, nano-imaging, nanorobots, and so forth, which allow for restrictions on the use of novel atherosclerotic drugs to be lifted. This paper reviews new perspectives on the targeted delivery of nanoparticles to blood vessels for the treatment of atherosclerosis in both systemic and local drug delivery. In systemic drug delivery, nanoparticles inhibit drug degradation and reduce systemic toxicity through passive and active pathways. To further enhance the precise release of drugs, the localized delivery of nanoparticles can also be accomplished through blood vessel wall injection or using endovascular interventional devices coated with nanoparticles. Overall, nanotechnology holds boundless potential for the diagnosis and treatment of atherosclerotic diseases in the future. [ABSTRACT FROM AUTHOR]

Background: This article explored the possibility that the Mpox virus (MPXV) may initiate or stimulate the consequences of vascular inflammation. In 1970, it was discovered that Macaca cynomolgus primates infected with MPXV also infected humans in the Democratic Republic of the Congo. Discussion: The study demonstrates that MPXV invades host cells via viral proteins and surface receptors, initiating the release of diverse inflammatory mediators such as IL‐1, IL‐6, TNF‐α, CCL2, CXCL2, CXCL8, CXCL10, and so forth probably through endothelial dysfunction by reactive oxygen species production. In general, these mediators have been found to contribute to vascular inflammation and the formation of atherosclerotic plaque at a later stage, which may contribute to the onset of vascular inflammation. Conclusion: The discussed association between vascular inflammation and Mpox has the potential to be an important finding in the field of vascular biology research. [ABSTRACT FROM AUTHOR]

Atherosclerosis is one of the most important problems of modern medicine. It involves changes in the structure and inner lining of the arteries. Studying chemical elements directly in vascular tissues allows understanding the mechanisms of evolvement of cardiovascular diseases, in particular, atherosclerosis. This study is aimed at developing the neutron activation technique for the analysis of atherosclerotic plaques formed at various stages of the atherosclerosis and studying their composition. The content of 13 elements in lipid, fibrous, ulcerated, and calcific plaques was determined using the developed method. It was established that upon evolving atherosclerosis, the content of a number of essential elements changes, the content of calcium, strontium, selenium, zinc and iron increases, and the bromine content decreases. Also, it was suggested that iron plays a role in the evolution of atherosclerotic vascular lesions. [ABSTRACT FROM AUTHOR]

This article discusses the relationship between microplastics and cardiovascular diseases, emphasizing the importance of considering coexisting environmental pollutants. While human studies have shown a link between microplastics and cardiovascular issues, it is crucial to recognize that microplastics do not exist alone in the real world and often serve as carriers for other contaminants. The composition of these coexisting contaminants can vary geographically, making it challenging to achieve consistent findings in human studies. The article suggests that assessing the adverse effects of microplastics on humans requires information from both experimental studies and epidemiological data, and alternative approaches to protection may be necessary. [Extracted from the article]

Background/Objectives: Both hypertension and carotid atherosclerosis are independent risk factors for cardiovascular disease. We aim to investigate the synergistic effects of hypertension and carotid plaques on cardiovascular events and all-cause mortality. Methods: A follow-up study was conducted at the Preventive Cardiology Department of Vilnius University Hospital Santaros Klinikos between 2012 and 2021. The study recruited participants aged 40–65 who did not have overt cardiovascular disease (CVD) and were part of the Lithuanian High Cardiovascular Risk primary preventive program. The study collected demographic and clinical data, including an ultrasound assessment of carotid plaque. Results: The participants were monitored for 4–10 years for CVD events and all-cause mortality. Among 6138 participants, 954 (16%) experienced CVD events. The presence of carotid plaque on both sides was significantly associated with CVD events, myocardial infarction, and all-cause mortality. However, the combination of hypertension and carotid plaque did not significantly increase the risk for CVD events or all-cause mortality. Conclusions: The risk of CVD events or all-cause mortality was not significantly increased by the combination of hypertension and carotid plaque. Cardiovascular events depend on the extent of atherosclerosis in the carotid arteries. [ABSTRACT FROM AUTHOR]

LOX-1, ORL-1, or lectin-like oxidized low-density lipoprotein receptor 1 is a transmembrane glycoprotein that binds and internalizes ox-LDL in foam cells. LOX-1 is the main receptor for oxidized low-density lipoproteins (ox-LDL). The LDL comes from food intake and circulates through the bloodstream. LOX-1 belongs to scavenger receptors (SR), which are associated with various cardiovascular diseases. The most important and severe of these is the formation of atherosclerotic plaques in the intimal layer of the endothelium. These plaques can evolve into complicated thrombi with the participation of fibroblasts, activated platelets, apoptotic muscle cells, and macrophages transformed into foam cells. This process causes changes in vascular endothelial homeostasis, leading to partial or total obstruction in the lumen of blood vessels. This obstruction can result in oxygen deprivation to the heart. Recently, LOX-1 has been involved in other pathologies, such as obesity and diabetes mellitus. However, the development of atherosclerosis has been the most relevant due to its relationship with cerebrovascular accidents and heart attacks. In this review, we will summarize findings related to the physiologic and pathophysiological processes of LOX-1 to support the detection, diagnosis, and prevention of those diseases. [ABSTRACT FROM AUTHOR]

Atherosclerosis, a complex metabolic-immune disease characterized by chronic inflammation driven by the buildup of lipid-rich plaques within arterial walls, has emerged as a pivotal factor in the intricate interplay between cancer and cardiovascular disease. This bidirectional relationship, marked by shared risk factors and pathophysiological mechanisms, underscores the need for a comprehensive understanding of how these two formidable health challenges intersect and influence each other. Cancer and its treatments can contribute to the progression of atherosclerosis, while atherosclerosis, with its inflammatory microenvironment, can exert profound effects on cancer development and outcomes. Both cancer and cardiovascular disease involve intricate interactions between general and personal exposomes. In this review, we aim to summarize the state of the art of translational data and try to show how oncologic studies on cardiotoxicity can broaden our knowledge of crucial pathways in cardiovascular biology and exert a positive impact on precision cardiology and cardio-oncology. [ABSTRACT FROM AUTHOR]

Background: Coronary artery diseases are condition arises due to the clogging of atherosclerotic plaque coronary artery of heart; results decrease in the blood flow to the heart muscles. Formation of atherosclerotic plaques is the major cause of coronary artery disease (CAD). Among the several cardiovascular diseases, coronary artery disease (CAD) is the most prominent and prevalent. Cardiac biomarkers have become frontline diagnostic tools for myocardial infarction (MI); clinicians can make faster diagnostic decisions and design a more effective treatment plan, which reduces mortality. Detection of cardiac biomarkers plays an increasingly important role in evaluating and diagnosing patients with chest pain. Micro-vascular complications are increasingly linked to chronic hyperglycemia. Meta analysis of ten likewise studies on type-II diabetes have shown a potential association among cardiovascular disease and glycated hemoglobin and that have highly significant association (18%) of cardiovascular diseases risk by every 1% of elevated glycated hemoglobin concentration. Materials and Methods: The total study group consists of 400 subjects, of which 200 premature coronary artery disease patients (cases) & 200 were healthy individuals (controls). Venous blood was used for analysis. Cardiac markers (Tropnin-I & Myoglobin) were done by Immunofluorescence & HbA1c was done by Ion exchange HPLC method Bio-Rad D-10 Analyzer. The data analysis was done by using mean, standard deviation & student t-test. Results: Trop-I (0.58 ± 0.48 vs. 0.02 ± 0.006), Ck-MB (39.1 ± 11.02 vs. 14.79 ± 4.0) & Myoglobin (84.01 ± 8.22 vs. 38.99 ± 7.06) were higher in CAD patients than control subjects. The HbA1c (6.51 ± 0.36 vs. 4.66 ± 0.41) was higher in CAD patients than control subjects. The level of serum cardiac markers & HbA1c were significantly increased in CAD patients as compared to healthy individuals. Conclusion: The present study concluded that increased level of cardiac markers & HbA1c in Premature CAD patients as compared to healthy individuals. [ABSTRACT FROM AUTHOR]

Atherosclerosis is the most common cause of cardiovascular diseases that contribute to the major morbidity worldwide, but still lacking of effective treatment strategy. Here, a hybrid cell is constructed for the sonodynamic effect promoted cell therapy of early atherosclerosis by fusing M2 macrophages with thylakoid (TK) membranes. After systemic administration, the obtained TK-M2 actively accumulates in the early atherosclerotic plaques, wherein M2 macrophages relieve the cholesterol accumulation and the inflammation in the foam cells. Meanwhile, the TK membranes decorated on the M2 macrophages exhibit both type I and type II sonodynamic effects under ultrasound (US) activation, inducing the direct apoptosis of foam cells. The cooperation of M2 and TK leads to significant outcome in eliminating atherosclerotic plaques without obvious side-effects, providing a new avenue for atherosclerosis treatment. [ABSTRACT FROM AUTHOR]

Aim: To evaluate the association between apical periodontitis (AP) and atherosclerotic cardiovascular disease (ASCDV). Methodology: A total of 65 periodontally and systemically healthy patients (age ≥ 40 years) were included in the study. Periapical status was assessed through dental examination and periapical radiographs; 33 subjects had AP (AP+), while 32 acted as control (AP−). Moreover, data regarding their periapical index (PAI) score and the Decayed, Missing, and Filled Teeth (DMFT) index were recorded. All subjects underwent echo‐colour Doppler assessment of carotid intima‐media thickness (CIMT), carotid plaques, degree of stenosis using the North American Symptomatic Carotid Surgery Trial (NASCET) method, maximum diameter of the abdominal aorta (maximum AA) and common iliac arteries (CIA) diameters. Furthermore, peripheral blood flow was also measured using the ankle‐brachial index (ABI). Simple and multiple regression analyses were performed. Results: Among AP+ patients, 57.58% disclosed at least one sign of subclinical carotid atherosclerosis. Multiple regression analysis identified AP as a significant risk indicator for carotid plaques [OR = 4.87 (1.27, 18.98; p =.021)] and marked carotid intima‐media thickenings (OR = 14.58 [1.22, 176.15], p =.035). A significant association was established between AP and other cardiovascular (CV) variables (CIMT, NASCET, and maximum AA). On the contrary, a higher PAI score does not correlate to increased odds of carotid alterations, and the presence of AP did not prove any significant change in CIA and ABI. No significant correlation was established between DMFT and other variables. Conclusions: Results from the current study highlight that the presence of AP may be regarded as a risk indicator for ASCVD, with AP being associated with 5‐fold increased odds of having carotid plaques and 15‐fold increased odds of having marked carotid intima‐media thickenings. Further studies should be conducted in order to verify whether AP treatment could be beneficial for ASCVD signs. [ABSTRACT FROM AUTHOR]

Aims: To explore the relationship between severe hypoglycemia (SH) and hypoglycemia awareness with preclinical atherosclerosis in type 1 diabetes (T1D). Materials and Methods: Cross‐sectional study in patients with T1D without cardiovascular disease (CVD), and with ≥1 of the following: ≥40 years, diabetic kidney disease, or ≥10 years of T1D duration with another risk factor. CVD risk was estimated with the Steno T1 Risk Engine (Steno‐Risk). Carotid plaque was evaluated using standardised ultrasonography protocol. Logistic regression models adjusted for CVD risk factors were constructed to test the independent associations with SH or hypoglycemia awareness assessed by the Clarke questionnaire (Clarke). The inclusion of SH and Clarke in Steno‐Risk was further evaluated. Results: We included 634 patients (52.4% men, age 48.3 ± 10.8 years, T1D duration 27.4 ± 11.1 years, 39.9% harbouring plaque). A stepped increase in the presence of plaque according to Steno‐Risk was observed (13.5%, 37.7%, and 68.7%, for low, moderate, and high risk, respectively; p < 0.001). SH history (OR 4.4 [1.3–14.6]) and Clarke score (OR 1.7 [1.2–2.2]) were associated with plaque in low‐risk patients (n = 192). Clarke score was also associated with plaque burden in low‐moderate‐risk participants (n = 436; ≥2 plaques: OR 1.2 [1.0–1.5], p = 0.031; ≥3 plaques: OR 1.4 [1.1–2.0], p = 0.025). The inclusion of SH and Clarke scores in Steno‐Risk significantly improved the identification of low‐risk individuals with atherosclerosis (area under the curve: 0.658 vs. 0.576; p = 0.036). Conclusions: In patients with T1D without an estimated high CVD risk, SH and hypoglycemia awareness assessment score were independently associated with preclinical atherosclerosis and improved identification of patients who would benefit from an intensive approach. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a leading cause of death in the world. A significant body of evidence suggests that inflammation and various players are implicated and have pivotal roles in the formation of atherosclerotic plaques. Toll-like receptor 4 (TLR4) is linked with different stages of atherosclerosis. This receptor is highly expressed in the endothelial cells (ECs) and atherosclerotic plaques. TLR4 activation can lead to the production of inflammatory cytokines and related responses. Lectin-like oxidized low-density lipoprotein-1 (LOX-1), an integral membrane glycoprotein with widespread expression on the ECs, is involved in atherosclerosis and has some common pathways with TLR4 in atherosclerotic lesions. In addition, proprotein convertase subtilisin/kexin type9 (PCSK9), which is a regulatory enzyme with different roles in cholesterol uptake, is implicated in atherosclerosis. At present, TLR4, PCSK9, and LOX-1 are increasingly acknowledged as key players in the pathogenesis of atherosclerotic cardiovascular diseases. Herein, we presented the current evidence on the structure, functions, and roles of TLR4, PCSK9, and LOX-1 in atherosclerosis. [ABSTRACT FROM AUTHOR]

People with type 1 diabetes (T1D) have a high cardiovascular disease (CVD) risk, which remains the leading cause of death in this population. Despite the improved control of several classic risk factors, particularly better glycaemic control, cardiovascular morbidity and mortality continue to be significantly higher than in the general population. In routine clinical practice, estimating cardiovascular risk (CVR) in people with T1D using scales or equations is often imprecise because much of the evidence comes from pooled samples of people with type 2 diabetes (T2D) and T1D or from extrapolations of studies performed on people with T2D. Given that T1D onsets at a young age, prolonged exposure to the disease and its consequences (e.g., hyperglycaemia, changes in lipid metabolism or inflammation) have a detrimental impact on cardiovascular health. Therefore, it is critical to have tools that allow for the early identification of those individuals with a higher CVR and thus be able to make the most appropriate management decisions in each case. In this sense, atherosclerosis is the prelude to most cardiovascular events. People with diabetes present pathophysiological alterations that facilitate atherosclerosis development and that may imply a greater vulnerability of atheromatous plaques. Screening for subclinical atherosclerosis using various techniques, mainly imaging, has proven valuable in predicting cardiovascular events. Its use enables the reclassification of CVR and, therefore, an individualised adjustment of therapeutic management. However, the available evidence in people with T1D is scarce. This narrative review provides and updated overview of the main non-invasive tests for detecting atherosclerosis plaques and their association with CVD in people with T1D. [ABSTRACT FROM AUTHOR]

Atherosclerosis, which currently contributes to 31% of deaths globally, is of critical cardiovascular concern. Current diagnostic tools and biomarkers are limited, emphasizing the need for early detection. Lifestyle modifications and medications form the basis of treatment, and emerging therapies such as photodynamic therapy are being developed. Photodynamic therapy involves a photosensitizer selectively targeting components of atherosclerotic plaques. When activated by specific light wavelengths, it induces localized oxidative stress aiming to stabilize plaques and reduce inflammation. The key advantage lies in its selective targeting, sparing healthy tissues. While preclinical studies are encouraging, ongoing research and clinical trials are crucial for optimizing protocols and ensuring long-term safety and efficacy. The potential combination with other therapies makes photodynamic therapy a versatile and promising avenue for addressing atherosclerosis and associated cardiovascular disease. The investigations underscore the possibility of utilizing photodynamic therapy as a valuable treatment choice for atherosclerosis. As advancements in research continue, photodynamic therapy might become more seamlessly incorporated into clinical approaches for managing atherosclerosis, providing a blend of efficacy and limited invasiveness. [ABSTRACT FROM AUTHOR]

Recent studies have shown that a pro-inflammatory diet and dysbiosis, especially a high level of trimethylamine-N-oxide (TMAO), are associated with various adverse health conditions. Cardiovascular diseases and pancreatic diseases are two major morbidities in the modern world. Through this narrative review, we aimed to summarize the association between a pro-inflammatory diet, gut microbiota, and cardiovascular and pancreatic diseases, along with their underlying mechanisms. Our review revealed that TMAO is associated with the development of cardiovascular diseases by promoting platelet aggregation, atherosclerotic plaque formation, and vascular inflammation. TMAO is also associated with the development of acute pancreatitis. The pro-inflammatory diet is associated with an increased risk of pancreatic cancer and cardiovascular diseases through mechanisms that include increasing TMAO levels, activating the lipopolysaccharides cascade, and the direct pro-inflammatory effect of certain nutrients. Meanwhile, an anti-inflammatory diet decreases the risk of cardiovascular diseases and pancreatic cancer. [ABSTRACT FROM AUTHOR]

Background: The pathogenesis of many syncopal episodes remains unexplained. Intestinal dysbiosis could be involved in the pathophysiological mechanisms of syncope due to its connection with the central nervous system via the microbiota–gut–brain axis. This pilot study aimed to explore the specific cardiometabolic risk factors and gut microbiota in unexplained syncope (US), compared to other types of syncope, to assess their similarity or verify their different origins. Methods: We studied 86 participants with syncope, who were divided into four groups: an orthostatic syncope group (OH, n = 24), a neuromediated syncope group (NMS, n = 26), a cardiological syncope group (CS, n = 9), and an unexplained syncope group (US, n = 27). We evaluated the anthropometric, clinical, and metabolic characteristics of the four groups; the α- and β-diversity; and the differences in the abundance of the microbial taxa. Results: The US group had a lower incidence of systolic hypertension at the first visit and a lower frequency of patients with nocturnal hypertension than the CS group. Compared to the OH and NMS groups, the US group had a higher incidence of carotid plaques and greater carotid intima–media thickness, respectively. The microbiota differed significantly between the US and CS groups, but not between the US group and the OH or NMS group. Conclusions: We observed significant differences in the gut microbiota between CS and US. Future studies are necessary to evaluate the involvement of the gut microbiota in the complex pathogenesis of syncope and whether its analysis could support the interpretation of the pathophysiological mechasnisms underlying some episodes classifiable as US. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a chronic inflammatory disease that affects arteries and is the main cause of cardiovascular disease. Atherosclerotic plaque formation is usually asymptomatic and does not manifest until the occurrence of clinical events. Therefore, early diagnosis and treatment of atherosclerotic plaques is particularly important. Here, a series of NIR‐II fluorescent dyes (RBT‐NH) are developed for three photoresponsive NO prodrugs (RBT‐NO), which can be controllably triggered by 808 nm laser to release NO and turn on the NIR‐II emission in the clinical medicine "therapeutic window". Notably, RBT3‐NO is selected for its exhibited high NO releasing efficiency and superior fluorescence signal enhancement. Subsequently, a platelet‐mimicking nano‐prodrug system (RBT3‐NO‐PEG@PM) is constructed by DSPE‐mPEG5k and platelet membrane (PM) for effectively targeted diagnosis and therapy of atherosclerosis in mice. The results indicate that this platelet‐mimicking NO nano‐prodrug system can reduce the accumulation of lipids at the sites of atherosclerotic plaques, improve the inflammatory response at the lesion sites, and promote endothelial cell migration, thereby slowing the progression of plaques. [ABSTRACT FROM AUTHOR]

Room‐temperature phosphorescent (RTP) materials have great potential for in vivo imaging because they can circumvent the autofluorescence of biological tissues. In this study, a class of organic‐doped long‐wavelength (≈600 nm) RTP materials with benzo[c][1,2,5] thiadiazole as a guest was constructed. Both host and guest molecules have simple structures and can be directly purchased commercially at a low cost. Owing to the long phosphorescence wavelength of the doping system, it exhibited good tissue penetration (10 mm). Notably, these RTP nanoparticles were successfully used to image atherosclerotic plaques, with a signal‐to‐background ratio (SBR) of 44.52. This study provides a new approach for constructing inexpensive red organic phosphorescent materials and a new method for imaging cardiovascular diseases using these materials. [ABSTRACT FROM AUTHOR]

Background: The basis for increased cardiovascular events following acute infection is hypothesized to be endothelial dysfunction, characterized by atheromatous plaque rupture and the development of a prothrombotic environment. As acute cardiovascular diseases (CVDs), specifically ischemic stroke and MI, are major causes of morbidity and mortality in the India and worldwide, understanding the basis for acute cardiovascular events and any potential for prevention becomes increasingly important. Aims and Objectives: To analyze the patients suffering from Herpes Zoster (Shingles) in correlation with cardiovascular diseases. Materials and Methods: Retrospective study was performed in our private clinics as well as in the department of Dermatology, General Medicine, Cardiology and Neuro-medicine, Santiniketan Medical College and Hospital, Bolpur, Birbhum, West Bengal, India. Sample subjects were 200, distributed in 2 separate group, Non HZ group and HZ group, 100 subjects in each group. Results and Observations: Overall, 200 subjects were diagnosed with HZ during the study period, 200 patients were included in this study (100 patients per group). The average age at zoster diagnosis was 45.7 (±18.0) years. Of these patients, 33.8 were male, 18% had diabetes mellitus, and 30.5% had hypertension as underlying diagnoses. The follow-up period did not differ significantly between the study groups, with a minimum of 0 and a maximum of 5 years, and a mean follow-up interval of 1.5 years. Cumulative MACCE survival at the end of the follow-up period was 54% in the HZ group as compared to 74% in the non-HZ group (P<0.001) Conclusion: Our study concluded as the risk of Major Adverse Cardiac and Cerebrovascular Events (MACCE) is higher by approx. 20% in 1st year of follow up (P<0.001) of patients among the Zoster group, therefore Herpes Zoster is a marker of long term cardio vascular diseases risks. [ABSTRACT FROM AUTHOR]